0022-5347 /78/1202-0511$02. 00/D
Vol. Printed
THE JOURNAL OF UROLOGY
Copyright © 1978 by The Williams & Wilkins Co.
Octobe, U.S.A.
Letters to the Editor NON-METASTATIC HEPATIC DYSFUNCTION
RE: MULTIPLE ENDOCRINE ADENOMATOSIS: IN SUPPORT OF THE COMMON ORIGIN THEORIES
To the Editor. We enjoyed reading the recent article by Boxer and associates.' Our-~xperience with hepatic dysfunction in patients with renal carcinoma but without hepatic metastases was published in 1973. 2 We presented the results of liver function studies in 40 cases of renal carcinoma without hepatic metastases. In 15 patients hepatic function studies were abnormal. The cause of this hepatic dysfunction in cases of non-metastatic renal carcinoma is unknown but, perhaps, an immunological factor could be involved. After 5 years of followup of our 15 patients we concluded that abnormal liver function tests have a prognostic significance in relation to the outcome of renal carcinoma. Thus, reversible liver dysfunction is a good prognostic sign and a survival rate of more than 5 years should be expected. Persisting liver dysfunction after nephrectomy indicated a poor prognosis. In the cases in which liver dysfunction disappeared after nephrectomy the reappearance of abnormal hepatic tests indicates the presence of metastases. Respectfully. C. Dimopoulos Universite D'Athenes Faculte De Medicine Chaire D'Urologie Hopital V. Paulos, Goudi Athens, Greece
K. L. Janson, J. A. Roberts and M. Varela
1. Boxer, R. J., Waisman, J., Lieber, M. M., Mampaso, F. M. and
Skinner, D. G.: Non-metastatic hepatic dysfunction associated with renal carcinoma. J. Urol., 119: 468, 1978. 2. Dimopoulos, C., Billis, A., Sideris, D., Dimopoulos, B., Doicas, J., Scouteris, M. and Gervas, A.: Interet de l'etude de la fonction hepatique au cours de l'evolution du cancer du rein. Ann. d'Urol., 7: 99, 1973.
TUMORS OF TESTIS IN ELDERLY MEN To the Editor. I read with interest the 2 most recent case reports on embryonal carcinoma of the testis in elderly men_l. 2 In the last 5 to 6 years I have reviewed tissue slides from 10 elderly patients who had orchiectomy for scrotal masses. In 5 cases a lymphoma was found. In 1 case this was a manifestation of spread to the testis from lymphoma elsewhere but in the remainder it seemed to be the only focus. There were some seminomas and embryonal carcinomas in the remainder. I am calling attention to this incidence of lymphoma of the testis in older men. It seems to be on the increase. Respectfully, Meyer M. Melicow Uropathology Research Columbia University College of Physicians and Surgeons New York, New York 10032 1. Tuttle, J. P., Jr., Pratt-Thomas, H. R. and Thomason, W. B.:
Embryonal carcinoma of the testis in elderly men. J. Urol., 118: 1070, 1977.
2. Morrow, T. W. and Soloway, M. S.: Embryonal carcinoma of the testis in elderly men: letter to the editor. J. Urol., 119: 709, 1978.
J. Urol., 119: 161-165, 1978 To the Editor. In their article Janson and associates imply that all endocrine cells secreting amines and polypeptides come from the neural crest. This is far from established and Pearse and associates 1 recently noted that sucli origin had been shown for only 6 of the 36 known constituents of the APUD system. For the APUD cells of the gut the evidence at present is against neural crest origin and can be summarized as follows: 1) embryologic;1 2) morphologic: local derivation of these cells has been demonstrated from the crypt enteroblast; 2 3) neoplastic: enteroblastic origin of the carcinoid precursor cell is favored by the intestinal mucocarcinoid3 and the secondary development of ovarian carcinoids from teratomatous endoderm 4 and 4) metaplastic: enterochromaffin cells are common in enteric metaplasia seen in chronic cholecystitis and pyocystis; their orderly disposition in harmony with the other metaplastic elements favors endodermal origin (personal observations). The APUD system is best viewed as an example of structuralfunctional convergence in evolutionary terms. As the prime controllers of organelle differentiation and synthesis of cell secretion, the genomes of these widely scattered and multiple derived APUD cells also have converged and developed functional similarities. I would like to propose that one of these similarities is a genetically determined and variably expressed predisposition to neoplasia, which underlies the morphologic and secretory spectrum of the pluriglandular syndromes. Respectfully, Louis Honore Grace General Hospital St. John's, Canada 1. Pearse, A. G. E., Polak, J. M. and Bloom, S. R.: The newer gut hormones: cellular sources, physiology, pathology and clinical aspects. Gastroenterology, 72: 746, 1977. 2. Ferreira, M. N. and Leblond, C. P.: Argentaffin and other "endocrine" cells of the small intestine in the adult mouse. II. Renewal. Amer. J. Anat., 131: 331, 1971. 3. Haqqani, M. T. and Williams, G.: Mucin producing carcinoid tumours of the vermiform appendix. J. Clin. Path., 30: 473, 1977.
4. Doucette, J. W. and Estes, W. B.: Primary ovarian carcinoid tumors. Case report and review of the literature. Obst. Gynec., 25: 94, 1965.
Reply by Authors. Perhaps this is a semantic problem. It seems we both agree that familial multiple endocrine adenomatosis is determined genetically. It recently has been shown very nicely that the initial event is a mutation producing multiple clones of cells susceptible to a second mutational event that may cause tumors in one or many glands. 1 Since this is so it would seem that the first event affected some common stem cell. Whether this cell is neuroectodermal is really unimportant. Although it could be in the case of apudomas cells of the gut, it certainly has not been proved. The importance of the apudoma concept is that it will increase our awareness of the possible presence of another endocrine tumor when one is found in a patient. Our family lends support to the theory. If a common etiologic origin exists we should expect to find other patients with overlap between the usual tumor groupings as we identified in this family. 1. Baylin, S. B., Hsu, S. H. and Gann, D. S.: Inherited medullary thyroid carcinoma: a final monoclonal mutation in one of multiple clones of susceptible cells. Science, 199: 429, 1978.
511
Vol. Printed
THE JOURNAL OF UROLOGY
Copyright © 1978 by The Williams & Wilkins Co.
Octobe, U.S.A.
Letters to the Editor NON-METASTATIC HEPATIC DYSFUNCTION
RE: MULTIPLE ENDOCRINE ADENOMATOSIS: IN SUPPORT OF THE COMMON ORIGIN THEORIES
To the Editor. We enjoyed reading the recent article by Boxer and associates.' Our-~xperience with hepatic dysfunction in patients with renal carcinoma but without hepatic metastases was published in 1973. 2 We presented the results of liver function studies in 40 cases of renal carcinoma without hepatic metastases. In 15 patients hepatic function studies were abnormal. The cause of this hepatic dysfunction in cases of non-metastatic renal carcinoma is unknown but, perhaps, an immunological factor could be involved. After 5 years of followup of our 15 patients we concluded that abnormal liver function tests have a prognostic significance in relation to the outcome of renal carcinoma. Thus, reversible liver dysfunction is a good prognostic sign and a survival rate of more than 5 years should be expected. Persisting liver dysfunction after nephrectomy indicated a poor prognosis. In the cases in which liver dysfunction disappeared after nephrectomy the reappearance of abnormal hepatic tests indicates the presence of metastases. Respectfully. C. Dimopoulos Universite D'Athenes Faculte De Medicine Chaire D'Urologie Hopital V. Paulos, Goudi Athens, Greece
K. L. Janson, J. A. Roberts and M. Varela
1. Boxer, R. J., Waisman, J., Lieber, M. M., Mampaso, F. M. and
Skinner, D. G.: Non-metastatic hepatic dysfunction associated with renal carcinoma. J. Urol., 119: 468, 1978. 2. Dimopoulos, C., Billis, A., Sideris, D., Dimopoulos, B., Doicas, J., Scouteris, M. and Gervas, A.: Interet de l'etude de la fonction hepatique au cours de l'evolution du cancer du rein. Ann. d'Urol., 7: 99, 1973.
TUMORS OF TESTIS IN ELDERLY MEN To the Editor. I read with interest the 2 most recent case reports on embryonal carcinoma of the testis in elderly men_l. 2 In the last 5 to 6 years I have reviewed tissue slides from 10 elderly patients who had orchiectomy for scrotal masses. In 5 cases a lymphoma was found. In 1 case this was a manifestation of spread to the testis from lymphoma elsewhere but in the remainder it seemed to be the only focus. There were some seminomas and embryonal carcinomas in the remainder. I am calling attention to this incidence of lymphoma of the testis in older men. It seems to be on the increase. Respectfully, Meyer M. Melicow Uropathology Research Columbia University College of Physicians and Surgeons New York, New York 10032 1. Tuttle, J. P., Jr., Pratt-Thomas, H. R. and Thomason, W. B.:
Embryonal carcinoma of the testis in elderly men. J. Urol., 118: 1070, 1977.
2. Morrow, T. W. and Soloway, M. S.: Embryonal carcinoma of the testis in elderly men: letter to the editor. J. Urol., 119: 709, 1978.
J. Urol., 119: 161-165, 1978 To the Editor. In their article Janson and associates imply that all endocrine cells secreting amines and polypeptides come from the neural crest. This is far from established and Pearse and associates 1 recently noted that sucli origin had been shown for only 6 of the 36 known constituents of the APUD system. For the APUD cells of the gut the evidence at present is against neural crest origin and can be summarized as follows: 1) embryologic;1 2) morphologic: local derivation of these cells has been demonstrated from the crypt enteroblast; 2 3) neoplastic: enteroblastic origin of the carcinoid precursor cell is favored by the intestinal mucocarcinoid3 and the secondary development of ovarian carcinoids from teratomatous endoderm 4 and 4) metaplastic: enterochromaffin cells are common in enteric metaplasia seen in chronic cholecystitis and pyocystis; their orderly disposition in harmony with the other metaplastic elements favors endodermal origin (personal observations). The APUD system is best viewed as an example of structuralfunctional convergence in evolutionary terms. As the prime controllers of organelle differentiation and synthesis of cell secretion, the genomes of these widely scattered and multiple derived APUD cells also have converged and developed functional similarities. I would like to propose that one of these similarities is a genetically determined and variably expressed predisposition to neoplasia, which underlies the morphologic and secretory spectrum of the pluriglandular syndromes. Respectfully, Louis Honore Grace General Hospital St. John's, Canada 1. Pearse, A. G. E., Polak, J. M. and Bloom, S. R.: The newer gut hormones: cellular sources, physiology, pathology and clinical aspects. Gastroenterology, 72: 746, 1977. 2. Ferreira, M. N. and Leblond, C. P.: Argentaffin and other "endocrine" cells of the small intestine in the adult mouse. II. Renewal. Amer. J. Anat., 131: 331, 1971. 3. Haqqani, M. T. and Williams, G.: Mucin producing carcinoid tumours of the vermiform appendix. J. Clin. Path., 30: 473, 1977.
4. Doucette, J. W. and Estes, W. B.: Primary ovarian carcinoid tumors. Case report and review of the literature. Obst. Gynec., 25: 94, 1965.
Reply by Authors. Perhaps this is a semantic problem. It seems we both agree that familial multiple endocrine adenomatosis is determined genetically. It recently has been shown very nicely that the initial event is a mutation producing multiple clones of cells susceptible to a second mutational event that may cause tumors in one or many glands. 1 Since this is so it would seem that the first event affected some common stem cell. Whether this cell is neuroectodermal is really unimportant. Although it could be in the case of apudomas cells of the gut, it certainly has not been proved. The importance of the apudoma concept is that it will increase our awareness of the possible presence of another endocrine tumor when one is found in a patient. Our family lends support to the theory. If a common etiologic origin exists we should expect to find other patients with overlap between the usual tumor groupings as we identified in this family. 1. Baylin, S. B., Hsu, S. H. and Gann, D. S.: Inherited medullary thyroid carcinoma: a final monoclonal mutation in one of multiple clones of susceptible cells. Science, 199: 429, 1978.
511
